Phthalates, Poison in Plastics

By Jared Boles, for Plastifree™

                If you’ve ever been in a store selling health and wellness products before, you’ve probably seen it before, that funny word which every label emphatically declares is nowhere in the ingredients, “phthalate”. Ffff…th….what?!  Pronounced “θæleɪt” (does that help?), phthalates are a family of clear liquid chemical additives commonly used in plastics as softeners and conditioners, and in personal care products like makeup as part of their base ingredients (1).  So why does every health company worth their organic Himalayan salt avoid phthalates like the plague?  As we’ll explore in this article, phthalates are toxic chemicals ubiquitous in the modern human environment of the Plastic Age, and their consequences to human and animal health need to come into the light for all to see.

                Each and every year, literally millions of tons of phthalates are produced globally for the plastics market (1, 2). When you understand the physical nature of plastics, the reality of the matter is scarier than just big numbers. Plastics, especially polyvinyl-chloride (PVC), are actually quite porous on a microscopic scale, and phthalates are not fully chemically bound to the plastics they modify. This means that the phthalate additives in plastics, anywhere from 20-60% of the product by weight, are slowly oozing toxins into the air you breathe, the water you drink, and into the products you enjoy (1,2). In fact, multiple studies have all confirmed that within the United States alone, metabolites of phthalate chemicals (their degraded chemical byproducts in the body) could be detected in the blood and urine of at least 95% of the population (2). A study in 2010 sought to measure phthalate leaching from just one of many common sources, namely the prominent PVC additive DEHP (di-2-ethylhexyl phthalate) emitted from common vinyl flooring (2,3). They found that the average vinyl flooring contains between 20-40% pure DEHP by weight in order to provide flexibility to the otherwise inherently brittle PVC. When the authors studied the actual routes and rates of exposure, the results were literally flooring. Of all the routes of intake analyzed, including vapor inhalation, particle inhalation, and dermal skin contact, the main path of transmission into the human body was through the unintentional ingestion of household dust. It was determined that dust acted as an effective carrier of DEHP absorbed from the vinyl flooring, and that particles suspended in the air would then be ingested and release the attached DEHP into the body. The effect of dust transfer was notably increased in the presence of indoor air circulation through household fans by raising the rate at which other household items were plastered with airborne chemical, and increasing the velocity at which the skin was hit with DEHP, which raised the dermal absorption rate approximately 13%. In the study, both adults and children were analyzed, with results echoing previous studies which showed dramatically differing daily intakes of phthalates from all sources depending on subject age, as children were found to absorb anywhere from 2 to 10 times more DEHP than adults, at least twice the EPA recommended daily maximum (2, 4). And it’s not just vinyl flooring that’s the culprit, since phthalates leach from so many plastic products that they can be absorbed through indoor and outdoor air, water sources, and even the soil can absorb and host phthalates (2, 7). A study in 2013 even examined how phthalates leached into food products just through the manufacturing process and storage in plastic-based containers alone; out of 72 assorted common consumables of all food groups purchased from multiple supermarkets in Albany, New York, 74% tested positive for DEHP, 57% for DEP(diethyl phthalate), 55% for DiBP (diisobutyl phthalate), 54% for BBzP (butyl benzyl phthalate), 37% for DMP (dimethyl phthalate), and 31% for DBP (di-n-butyl phthalate) (4).  You might be wondering at this point, why is this all important? What’s so bad about phthalates that it matters how much the kids are getting into? Well, numerous studies conducted over the years conclusively show that phthalates are harmful to humans and animals alike; unfortunately, unless you spend most of your day in a white lab coat, you’ve probably never even heard of the studies. In the interest of brevity, and for the sake of everyone’s sanity, we’ll briefly cover just a few of the major studies that illustrate the main dangers of phthalate exposure through plastics.

                As we just learned from the study above, phthalates from vinyl flooring, just one of the many sources of plasticizers we come into contact with every day, are absorbed by children in amounts at least double that of adults.  A recent 2018 study for Environmental Health hypothesized that the type and amount of phthalates within pregnant mothers may have a positive correlation with the incidence of autism spectrum disorders in their children. When the results were in, they couldn’t definitively say they found the smoking gun, but they certainly found some shady chemicals of interest. “Results from this study did not support our hypothesis that phthalate exposures during mid- to late pregnancy are associated with an increased risk of having a child with ASD [autism spectrum disorder] in overall analyses, but showed that exposures to some phthalates may increase risk of having a child with Non-TD[non-typical cognitive development].” In the study, 201 expecting mothers evaluated as having a high-risk history for infant autism submitted urine samples during the second and third trimesters of pregnancy which were analyzed for levels of any of 14 metabolite byproducts of 8 different common phthalates. At three years of age, the children were tested for ASD and classified as either typical development (TD, n=100), non-typical development (Non-TD, n=55), or ASD (n=46). By comparing prenatal phthalate exposure based on the metabolites detected in the mother’s urine, and the results of the children’s ASD screening at three years of age, the researchers were able to make some clear connections between the mother’s phthalate levels and whether her child developed atypical cognitive development. What they found was that results were split for currently unknown reasons along gender lines, and that only boys showed any clear relation between prenatal phthalate exposure and Non-TD. Of the handful of phthalate metabolites positively associated with Non-TD, monoethyl phthalate (MEP) showed the most dramatic correlation, especially when the moment of greatest exposure occurred during the third trimester. Other metabolites could also be tied to greater risk of Non-TD to a less obvious degree, but it was found that these metabolites (MCPP, MCOP, and MCNP) were only tied to Non-TD in children whose mothers did not take multivitamins during pregnancy. This remarkable relation between impaired cognitive development and nutrition, the researchers theorized, could be due to a recorded link between phthalates like DEHP and resultant deficiencies in vitamin D and zinc, along with documented maternal inflammatory responses that may deplete anti-inflammatory vitamins B, C, D, and E in response. Without these nutrients available to the developing baby, inflammation could potentially impact brain tissue and lead to effects like Non-TD (5).  Clearly all the more reason for expecting mothers (and everyone for that matter) to make sure they’re getting a healthy diet, plenty of vitamins, and staying away from toxin-laden plastics.

                So, we haven’t quite found the 100% sure source of autism just yet but, clearly, studies are finding a connection between phthalate exposure in mothers and a resulting decrease in cognitive development that is detected in their children using the exact same tests used to diagnose autism. That should scare each and every one of us, considering the potential damage to future generations and the damage already done to innocent children struggling to make their way in the world today. What’s more, research shows that brain development isn’t the only thing being affected by phthalates in the womb.  In 2017 a study funded by the U.S. Environmental Protection Agency and National Institute of Environmental Health Sciences sought to expand on previous studies showing a potential connection between prenatal phthalate exposure and the eventual development of childhood obesity. In the study, 345 expecting mothers completed a program where urine samples taken at the end of the first and second trimesters were evaluated for the presence of any of 11 possible metabolites of 8 different phthalates absorbed from their everyday environment.  The results of these urine tests were later compared with the children’s BMI, waist circumference, and percentage of body fat at ages 5, 7, 9, 10.5, and 12 (6). The findings of this study, while over a decade in the making and covering a wide array of variables, was summarized surprisingly succinctly by the authors:

We found that higher concentrations of urinary MEP, MBzP [monobenzyl phthalate], and ΣDEHP[DEHP] metabolites in pregnant mothers were associated with increased odds of their children being overweight or obese between 5 and 12 years of age. Higher prenatal MEP concentrations were consistently associated with increased BMI, waist circumference, and percent body fat in children between 5 and 12 years of age. Higher prenatal MBP [mono-n-butyl phthalate], MBzP, and ΣDEHP concentrations were also associated with larger body size over the same time period but less consistently. Results were similar at multiple ages between 5 and 12 years of age, suggesting that onset of puberty did not affect our findings. In addition, unlike previous studies, our results were quite similar between boys and girls. We saw some evidence of sex interaction with MBP and MCPP [mono (3-carboxypropyl) phthalate], with boys showing stronger positive associations with body size than girls, but not with other metabolites (6).

These results warrant further research, as the actual chemical mechanics behind how phthalates affect childhood BMI are currently not fully understood.  It is possible that learned lifestyle choices of the children, such as eating too much too often, or eating fast food more than healthy home-cooked meals could be partly to blame. Indeed, the authors noted that other studies show people who ate more fast food had higher levels of urinary phthalate metabolites due to processing and packaging of food products in and around plastics like PVC. Could mothers who ate lots of fast food have just taught their children to do the same, leading to weight problems? This is certainly very possible, indeed very likely in the case of families who do eat fast food regularly. However, the authors weren’t convinced this was an explanation that fit across the board, and the relations between certain phthalates and later obesity were just too well defined. Some theories they presented are based on the results of previous studies with both human and animal subjects, namely the role of DEHP in the development of hypothyroidism, and the antiandrogenic/estrogenic hormonal properties shown in at least some phthalates.  Hypothyroidism causes imbalance in thyroid hormone levels, leading to energy metabolism imbalance which can impact resting energy expenditure and increase fatty tissue growth. Imbalance of sex hormones can also lead to excess fat development, as the suppression of male hormones by phthalates can delay and impair puberty in boys, leading to spiked estrogen levels coupled with the added estrogenic effect of the  phthalates themselves promoting decreased muscle mass and increased fat deposits(6). In girls, the hormonal effects of phthalates have been tied to early puberty, weight gain, and shortened pregnancies (4, 6). In fact, a separate study observing the effects of DEHP on primate subjects found that female marmosets subjected to regular doses exhibited increased levels of the female hormone estradiol and showed heavier than normal ovarian and uterine weights; inversely, males in the study showed a significant decrease in testicular zinc content essential to sperm production  (7). Studies using rats have also noted traumatic damage to the male reproductive system, including decreased testicular weight, tubular atrophy, and increases in estradiol levels resulting from impaired liver function due to damage caused by supplementation of DEHP in the diet. (4,7). In human males, studies way back in 2003 and 2005 respectively found associations between phthalate exposure and damage to sperm cell DNA in men, and decreased anogenital distance in infant boys (4, 8, 9). That’s right, phthalate containing products threaten the very building blocks of the human body prior to conception, sabotage our children’s development in the womb, impair their ability to thrive socially and economically, and increase the risk of putting us all in the ground at a young age with organ damage and cancer. Oh, we didn’t mention the cancer?  Oh yeah, we’re dying to tell you about it!

          Cancer is by far one to the greatest scourges to human health in our era of poisons and plastics. It seems like every family is touched by it, and many are shattered by it. While the list of potential causes is long, and the numbers of carcinogens floating around in the modern environment are near innumerable, we’ll continue specifically to focus on the destructive role of phthalates released from common plastics and personal care products. On that note, current studies in both animal and human subjects show a defined relation between phthalate plasticizer exposure and increased risk of cancer in both newborn babies and adults. As we noted earlier, phthalates have been linked to preterm infant delivery which may be caused by resulting hormonal imbalance. At birth, a premature baby can expect to spend weeks in the hospital as they continue to grow and prepare for life outside plastic NICU incubators. And here is where baby’s first contact with plastics can be the most dangerous; several studies have noted a definite link between the amount of time a newborn spends in the NICU and both the rate and severity at which newborns experience cholestasis (usually temporary impairment of liver function resulting in jaundiced yellow skin) and hepatoblastoma (a childhood form of liver cancer)(7). One study in particular examined the rate at which infants receiving nutrition through PVC-containing systems developed cholestasis vs. those fed through systems that were PVC free (and also DEHP free). They determined that the rate of cholestasis was 50% through the PVC system and only 13% in the system that was PVC-free (10). These results were echoed in other studies using marmosets which sought to imitate the conditions human patients experience when undergoing regular blood transfusions through PVC tubing with DEHP as the plasticizer. After one year of treatment these studies found that liver function was abnormal, cholestasis was noted in at least some of the subjects, and that after a full 26 months without treatment liver function was still impaired and the structure of the liver cells themselves was abnormal (giant cells with more than one nucleus, for instance) (7). In rodents, several studies administering DEHP have found damage to and increased size of the liver, excessive liver enzymes indicating potential cancerous conditions, and tumors of the pancreas and testes(7). One of these studies, way back in 1987, administered DEHP to lactating females and found at least some abnormal changes transferred to the livers of suckling pups, with much worse damage to the mothers (11). While cancer studies with adult humans have been less conclusive, due in part to the clear legal and moral barriers to purposefully exposing people to harmful chemicals in a controlled scientific setting (but our exposure in the real world is ok, right?), Ivan Rusyn and J. Christopher Corton note in their 2012 EPA study of DEHPs role in the cancer epidemic  that the sum of human studies that have been attempted “infer possible associations of exposure to DEHP or other chemicals present in polyvinyl chloride[PVC]-containing  products with excess mortality from pancreatic, testicular, and respiratory tract cancers, excess incidence of multiple myeloma, as well as increased risk of breast cancer and pediatric hepatoblastoma” (7).

          Clearly researchers have known the damaging effects of phthalate plasticizers for decades now, and continue to discover more and more toxic side-effects every year, and yet how much of this did you already know? Likely not much, because to know is not only to fear, but also to be angry and to change lifestyles and buying habits which on a grand scale challenge the global economic status-quo. The economy depends on the consumer, and when the consumer’s best interests are not met in the products of that economy, the consumer takes their money elsewhere. Manufactures can do all of us one huge, very important favor and move to plastic-free alternatives. The character of humanity, down to our very genetic coding, is at stake. In the principle of supply-and-demand, the greater the economic demand, the more that need will be supplied. This principle is as reasonable as it is unchanging. In order to remove the toxic nature of plastics, we must change what we demand of the supply. If you vote with your dollar, and demand a higher standard of products free of plastics just like they were made in “the good ‘ol days”, suppliers will quickly notice a change and a strong new market will emerge to meet your demands. It’s self-interested, but the system works, provides employment, and can make our world healthy once again. We see the problem, it’s time to demand more, and to inform others; it’s time to do something about it!

Sources

• Phthalate. (2019, October 2). Retrieved November 3, 2019 from https://en.wikipedia.org/wiki/Phthalate

• Xu, Y., Cohen, H., Little, J. (2010, February 1). Predicting residential exposure to phthalate plasticizer emitted from vinyl flooring: sensitivity, uncertainty, and implications for biomonitoring. Environmental Health Perspectives, 118(2):253-8. Doi: 10.1289/ehp.0900559. Retrieved from https://ehp.niehs.nih.gov/doi/10.1289/ehp.0900559

• Bis(2-ethylhexyl) Phthalate. (2019, October 17). Retrieved November 3, 2019 from https://en.wikipedia.org/wiki/Bis(2-ethylhexyl)_phthalate

• Schecter, A., Lorber, M., Guo, Y., Wu, Q., Yun, S.H., Kannan, K., Hommel, M., Imran, N., Hynan, L.S., Cheng, D., Colacino, J., Birnbaum, L. (2013, April). Phthalate concentrations and dietary exposure from food purchased in New York State. Environmental Health Perspectives, 121 (4): 473-479. Doi:  10.1289/ehp.1206367. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3620091/

• Shin, H., Schmidt, R., Tancredi, D., Barkoski, J., Ozonoff, S., Bennett, D., Hertz-Picciotto, I. (2019, December 5). Prenatal exposure to phthalates and autism spectrum disorder in the MARBLES study. Environmental Health, 17: 85. Doi: 10.1186/s12940-018-0428-4. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6280477/

• Harley, K., Berger, K., Rauch, S., Kogut, K., Birgit Claus, H., Calafat, A., Huen, K., Eskenazi, B., Holland, N. (2017, September 1). Association of prenatal urinary phthalate metabolite concentrations and childhood BMI and obesity. Pediatric Research, 82(3): 405-415. Doi: 10.1038/pr.2017.112. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5581502/

• Rusyn, I., and Christopher Corton, J. (2012, April). Mechanistic considerations for human relevance of cancer hazard of di (2-ethylhexyl) phthalate . Mutation Research – Reviews in Mutation Research, 750(2): 141-158. Doi: 10.1016/j.mrrev.2011.12.004. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3348351/

• Duty, S.M., Singh, N.P., Manori, S.J., Barr, D.B., Brock, J.W., Ryan, L., Herrick, R.F., Christiani, D.C., Hauser, R. (2003, July). The relationship between environmental exposures to phthalates and DNA damage in human sperm using the neutral comet assay. Environmental Health Perspectives, 111(9): 1164-1169. Doi: 10.1289/ehp.5756. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1241569/

• Swan, S.H., Main, K.M., Liu, F., Stewart, S.L., Kruse, R.L., Calafat, A.M., Mao, C.S., Redmon, J.B., Ternand, C.L., Sullivan, S., Teague, J.L. (2005, August). Decrease in anogenital distance among male infants with prenatal phthalate exposure. Environmental Health Perspectives, 113(8): 1056-1061. Doi: 10.1289/ehp.8100. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1280349/

• von Rettberg, H., Hannman, T., Subotic, U., Brade, J., Schaible, T., Waag, K.L., Loff, S. (2009, August). Use of di(2-ethylhexyl)phthalate-containing infusion systems increases the risk of cholestasis. Pediatrics, 124(2):710-6. Doi: 10.1542/peds.2008-1765. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/19651587/

• Dostal, L.A., Weaver, R.P., Schwetz, B.A. (1987, December). Transfer of di(2-ethylhexyl) phthalate through rat milk and effects on milk composition and the mammary gland. Toxicology and Applied Pharmacology, 91(3):315-25. Doi: 10.1016/0041-008x(87)90054-8.